The morphologic features and physiologic mechanisms which are responsible for the recovery process following acute renal injury will be studied. The models to be used will include acute renal failure, induced by renal artery occlusion, and acute renal injury following acute unilateral or bilateral ureteral obstruction. It is proposed to study and define the mechanisms of recovery of single nephron function and glomerular filtration dynamics following an ischemic renal insult, as well as to investigate the specific mechanisms by which adenine nucleotides-MgCl2 have been effective in accelerating the recovery from acute renal failure. Studies will also be performed to establish the hemodynamic and morphologic features of the injury during complete ureteral occlusion and to modify the course of recovery following such an injury. The preferential recovery of superficial nephrons will be investigated in an attempt to determine whether this recovery is enhanced by alterations in blood flow or differential susceptibility of these nephrons to injury and resolution. Both physiologic and norphologic techniques will be used to study the differences in nephron populations and nephron segments. The possible effects of adenine nucleotides MgCl2 via alterations of vascular tone, restoration of cellular metabolism and reconstitution of cellular membranes will be investigated. Studies of acute renal failure following ureteral obstruction will be parallel to those of ischemic injury with attempts to elucidate whether vascular or cellular events predominate in this form of injury.